I investigate models of the spread of transposable elements, such as the Drosophila melanogaster P elements, that can exist in autonomous and non-autonomous forms. Elements which have their major impact on host fitness in the process of transposition can, under certain conditions, come to a stable balance between transposition and selection. This stable balance for autonomous elements can be disrupted by the invasion of further elements, which do not produce a transposase enzyme, and may produce a repressor of transposition. I examine this secondary invasion process, and show that a stable equilibrium copy number for intact elements is neither a necessary nor a sufficient condition for non-autonomous elements to invade. Nevertheless, invasion occurs under a broad range of models and conditions. This requires neither that the non-autonomous elements produce a trans-acting repressor of transposition, nor that they titrate transposase. The elimination of autonomous elements follows the increase in non-autonomous elements unless the latter encode powerful repressors of transposition. Approximate solutions for the equilibrium copy number of autonomous elements and rate of invasion of non-autonomous elements can be found under some models for transposition and selection. The predictions of the model are compared with recent empirical studies of the D. melanogaster P system

7-tricosene (7-T) and 7-pentacosene (7-P) are the two main hydrocarbons on the cuticle of male Drosophila melanogaster. These two substances might play a pheromonal role during courtship behaviour. We investigated the genetic basis of the quantitative polymorphism observed in the production of 7-T and 7-P. Strains of different geographic origin, with males producing either predominantly 7-T or predominantly 7-P, were hybridized with strains carrying genetic markers. We found that chromosome II changes the balance between 7-T and 7-P while chromosome III regulates the overall quantity of both 7-monoenes. We have also characterized and roughly mapped sept and smoq, two genetic factors on chromosome II that act additively on the production of both cuticular hydrocarbons. The genetic control of the variation in 7-T and 7-P varies between D. melanogaster strains and between D. melanogaster and its sibling species D.simulans. The possible evolutionary and physiological causes of this variation as well as its functional implication for courtship behaviour are discussed.

Currently in the hobo system of hybrid dysgenesis, strain classification is based on the presence/absence of the 2·6 kb Xho I restriction fragment. Using this criterion, strains are classified as: (1) H strains when full-size elements are detected by presence of a 2·6 kb Xho I restriction fragment; they can also contain internally deleted elements; (2) DH strains when only deleted elements are detected (Xho I restriction fragment less than 2·6 kb); (3) E strains, devoid of any restriction fragment equal to or less than 2·6 kb in length. In addition, the strains can be classified on their ability to generate gonadal atrophy (GD sterility) when males of a studied strain are crossed with females from an E strain (dysgenic cross). Here we try to define the nature of the dysgenic cross, which leads us to analyse the different components of the dysgenic syndrome and to look for eventual correlations between them. Molecular analysis, GD sterility tests, hobo mobilization with the haw strain and the vgal strain, and hereditary transmission of the instability at the vg locus have been assayed in different strains. We show that the occurrence of GD sterility depends on the tested H strains as expected, but also on the E strains used. On the other hand we do not find any correlation between the different dysgenic parameters. Our data reveal that molecular and GD sterility tests are not sufficient to classify strains in the hobo system, and that all the components of the dysgenic syndrome must be taken into account. Our results are discussed with regard to active and full-size elements in relation to the structure of the S region where an amino acid sequence (TPE) presents a repetition polymorphism

In this paper we report on the diversity and distribution of a set of non-LTR retrotransposon (RTP) reverse transcriptase (RT) sequences isolated from phlebotomine sandflies, and their potential for investigating the evolutionary histories of members of this subfamily of flies (Diptera: Psychodidae, Phlebotominae). The phlebotomine RT sequence families derived from one species were as different from each other as they were from RT sequences derived from other species. When each was used to probe Southern blots of sandfly genomic DNA they hybridized only to the species of source and, usually, to others of the same subgenus, but not to DNA from other subgenera — a hybridization pattern consistent with vertical evolution. There was considerable intraspecific variation in hybridization pattern, suggesting the RTs were part of non-LTR RTPs that are (or were recently) subject to flux in genomic position and copy number. Most of the RT families detected in phlebotomines are monophyletic with respect to previously described RTs, and all are monophyletic with RTs of the F/Jockey (Drosophila melanogaster) type of RTP. Orthologous sequences were isolated from the closely related species Phlebotomus perniciosus and P. tobbi (subgenus Larroussius), and different populations of P. perniciosus. The level of sequence divergence among these orthologous RTs, the subgeneric distribution of each RT family, and the intraspecific variation in hybridization pattern of many of them, indicate this class of sequence will provide genetic markers at the sub-generic level.

Frequencies of anaphase I nondisjunction, germ cell death and pairing abnormalities at pachytene were assessed in male mice singly heterozygous and homozygous for the Robertsonian (Rb) translocations: Rb (1.3)lBnr, Rb(ll. 13)4Bnr and Rb(10. ll)8Bnr. Rb homozygotes showed low frequencies of nondisjunction but substantial germ cell death. This germ cell death could not be attributed to problems at pachytene as Rb homozygotes showed no increase in pairing abnormalities over the (C3H/HeH×1O1/H)F1 controls. Instead genie factors are involved. Rb heterozygotes showed substantial frequencies of nondisjunction and even greater germ cell death than found in the homozygotes. Pachytene pairing abnormalities were observed and it appears that these, together with genie factors, cause physiological perturbation of meiocytes, thereby promoting germ cell death, with nondisjunction of the trivalent as a sublethal response.

The t-complex on mouse chromosome 17 results in transmission ratio distortion in males heterozygous for complete haplotypes, and sterility in those homozygous for semi-lethal or doubly heterozygous for complementing lethal haplotypes. This sterility is due to inability of spermatozoa to fertilize. The haplotype th7 is an unusual laboratory-derived haplotype, postulated to carry a small duplication of t chromatin. Males heterozygous for th7 show a new form of sterility, apparently due to failure to form copulation plugs during mating. This is accompanied by a strong propensity to acute urinary obstruction. It is suggested that both the failure to form copulation plugs and the urinary obstruction are due to some abnormality in function of the accessory sex glands, and are the result of incorrect dosage of a gene in the postulated duplication. The symbol Msu for male sterility and urinary obstruction is suggested for the locus concerned. Previously a recessive form of abnormal behaviour had also been attributed to this duplication.

We investigated the interaction of recombination and selection on the process of fixation of two linked loci with epistatic interactions in fitness. We consider both the probability of fixation of newly arising mutants (the static model) and the time to fixation under continued mutation (the dynamic model). Our results show that the fixation of a new advantageous combination is facilitated by higher fitness of the advantageous genotype and by weaker selection against the intermediate deleterious genotypes. Fixation occurs more rapidly when the recombination rates are small, except when selection against intermediate genotypes is weak and selection in favour of the double mutant is very strong. In these cases fixation is more rapid when the recombinant rate is large. Mutations of strong effects, deleterious when alone but beneficial when coupled, are fixed more easily than mutations of intermediate effects, at least for large recombination rates. Among the possible pathways the process of fixation might follow, independent substitutions lead to the fixation of the double mutant only when selection is weak. The relative importance of the other pathways depends on the interaction between recombination and selection. The coupled-gamete pathway (i.e. when the population waits until the double mutant appears and then drives it to fixation) is more important as selection intensity increases and the recombination rate is reduced. For all recombination rates, asymmetries in fitness of the intermediate genotypes increase the rate at which fixations occur. Finally, throughout the fixation process, the population will be monomorphic at least at one of the two loci for most of the time, which implies that there would be little opportunity to detect the presence of negative epistasis even if it were important for occasional evolutionary transitions.

In highly integrated genetic systems, changes in any one component may have a deleterious effect on fitness, but coordinated, or compensatory, change in these components could lead to an overall increase in fitness compared with the current state. Wright designed his shifting-balance theory to account for evolutionary change in such systems, since natural selection alone can not lead to the new optimal state. A largely untreated aspect of the shifting-balance theory, that of the limiting impact of waiting for the production of new mutations, is analysed here. It is shown that the average time to double fixation of compensatory mutations is extremely long (of the order of tens or hundreds of thousands of generations), because selection is too effective in large populations, and mutations are too rare in small populations. Further, the probability that a new mutant will arise and undergo fixation quickly is extremely small. Tight linkage can reduce the time to fixation somewhat, but only in models in which the double heterozygote does not have reduced fitness. It is argued that the only reasonable way for compensatory mutations to become fixed in a population is if the new mutants are first allowed to achieve a moderate frequency through the relaxation of selection. Under these conditions, the time required to reach fixation is reasonably low, althoug the probability of being fixed is still small when the initial allele frequencies are low. It is likely that the waiting time for fixation of new mutants, which is here called phase zero, is the major limiting factor for the success of the shifting-balance process

Highly variable DNA polymorphisms called microsatellites are rapidly becoming the marker of choice in population genetic studies. Until now, microsatellites have not been utilized for Drosophila studies. We have identified eight polymorphic microsatellite loci in Drosophila melanogaster and used them to characterize the genetic variation in a wild population from the Tyrrell's winery in Australia. Microsatellites were isolated from a partial genomic DNA library. All microsatellites consist of (AC)n repeats ranging from n = 2 to n = 24. Six loci were assigned to chromosomal location by genetic mapping, with three loci on chromosome II, one locus on chromosome III and two loci on the X chromosome. Up to four microsatellite loci were multiplexed in the same reaction. Microsatellite variation is substantially greater than allozyme variation in the Tyrrell's Drosophila population. 80% of the microsatellite loci examined are polymorphic, compared with 28% of allozymes. The mean number of alleles per polymorphic locus is 5·2 in microsatellites compared with 30 in allozymes. The average observed heterozygosity of polymorphic microsatellites is 47% compared with 26% for allozymes. Microsatellite variation in Drosophila melanogaster is similar to that reported for other insects. Higher variability commends microsatellites over allozymes for genetic studies in Drosophila melanogaster.